Mahasweta Girgenrath, Ph.D.
Research Scientist
Skeletal muscle, neuromuscular disease, adult stem cell
Email: girgenrath at bbri.org

Research Summary
Muscular dystrophies are characterized by severe muscle degeneration and in some extreme forms result in a drastically shortened life span.  Many of these diseases are a result of partial or complete absence of proteins associated with the dystrophin-glycoprotein complex (DGC) at the sarcolemma (plasma membrane) of muscle cells. The DGC plays a role in providing a physical link between the intracellular myofibrilar structures with the extracellular matrix. We focus on the mechanisms that regulate skeletal muscle growth, repair, and survival in the context of muscular dystrophies. Particularly, we are interested in the role of apoptosis in muscle loss. Additionally, we are interested in mechanisms that dictate the self-renewal and proliferative capacity of muscle precursor cells and the factors that may influence these processes.

Selected Publications
Girgenrath, M., Kostek, C.A., and Miller. J.B. (2005) Diseased muscles that lack dystrophin or laminin-alpha2 have altered compositions and proliferation of mononuclear cell populations. BMC Neurol 7;5(1):7.

Girgenrath, M., Dominov, J.A., Kostek, C.A., Miller, J.B. (2004) Inhibition of apoptosis improves outcome in a model of congenital muscular dystrophy. J Clin Invest 114(11):1635-9.

Nowak , J, Malowitz , J., Girgenrath , M., Kostek , C., Kravetz , A., Dominov , J., andMiller, J. (2004). Immortalization of mouse myogenic cells can occur without loss of p16INK4a, p19ARF, or p53 and is accelerated by inactivation of Bax.. BMC Cell Biology, 5:1.

Girgenrath, M. and Marsh, R. L. (2003) Season and testosterone affect contractile properties of fast calling muscles in the gray tree frog Hyla chrysoscelis. Am J Physiol Regul Integr Comp Physiol 284(6):R1513-20.

PubMed:
Click here for a list of publications (searches the National Library of Medicine's PubMed database.)